Id1和HtrA1在卵巢上皮癌组织中的表达及临床意义
发布时间:2018-12-14 18:13
【摘要】:目的 探讨卵巢癌、良性卵巢肿瘤和正常卵巢组织中Id1(inhibitor of differentiation or DNA bindingl)和HtrA1(high temperature requirement factorl)的表达及其与临床病理参数的关系。 方法 (1)收集青岛大学医学院附属医院妇科40例卵巢上皮癌组织(化疗敏感组:20例、耐药组:20例)、10例良性卵巢肿瘤组织及10例正常卵巢组织。 (2)应用免疫组化SP的方法检测Id1和HtrA1在上皮性卵巢癌、良性卵巢肿瘤及正常的卵巢组织中表达。 (3)统计病人的年龄、肿瘤大小、术前CA125值、术前腹水量、肿瘤的组织学类型、病理分级程度、临床分期及其淋巴结的转移情况,并观察上述临床病理参数与Idl和HtrA1的表达的关系。 (4)探讨卵巢上皮癌组织中Id1和HtrA1的表达关系。 结果 (1)卵巢癌组织中Id1的表达阳性率为77.5%,明显高于良性卵巢肿瘤组织(40%,P0.05)和正常卵巢组织(30%,PO.05)。卵巢癌组织中HtrA1表达阳性率为22.5%,明显低于良性卵巢肿瘤组织(40%,P0.05)和正常卵巢组织(60%,P0.05)。 (2)卵巢癌耐药组中Id1阳性表达率为95%明显高于敏感组(60%,P0.05)。卵巢癌耐药组中HtrA1阳性表达率为5%明显低于敏感组(40%,P0.05)。 (3)患者术前CA125水平、病理分级和淋巴结转移分别与Idl和HtrA1的表达密切相关(P0.05)。 (4)Idl和HtrA1的表达呈负相关(r=-0.186,P=0.045)。 结论 (1)正常卵巢和良性卵巢肿瘤组织Id1阳性表达率较低,卵巢癌组织中阳性表达率较高,随组织恶变其表达率明显升高。而HtrA1则随组织恶变表达降低。 (2)随着卵巢上皮癌组织中Id1表达升高和HtrA1的表达降低,耐药性增加。 (3)Id1高表达和HtrA1低表达与卵巢上皮癌的化疗耐药及预后关系密切。
[Abstract]:Objective to investigate the expression of Id1 (inhibitor of differentiation or DNA bindingl) and HtrA1 (high temperature requirement factorl) in ovarian carcinoma, benign ovarian tumor and normal ovarian tissue and their relationship with clinicopathological parameters. Methods (1) 40 cases of ovarian epithelial carcinoma (chemosensitive group: 20 cases, drug-resistant group: 20 cases), 10 cases of benign ovarian tumor tissue and 10 cases of normal ovarian tissue were collected. (2) the expression of Id1 and HtrA1 in epithelial ovarian carcinoma, benign ovarian tumor and normal ovarian tissue were detected by immunohistochemical SP method. (3) the patient's age, tumor size, preoperative CA125 value, preoperative ascites volume, histological type of tumor, pathological grade, clinical stage and lymph node metastasis were analyzed. The relationship between the above clinicopathologic parameters and the expression of Idl and HtrA1 was observed. (4) to investigate the expression of Id1 and HtrA1 in epithelial ovarian carcinoma. Results (1) the positive rate of Id1 expression in ovarian cancer tissue was 77.5, which was significantly higher than that in benign ovarian tumor tissue (40 ovarian tumor tissues) and normal ovarian tissue (30jiao. 05). The positive rate of HtrA1 expression in ovarian cancer tissues was 22.5%, which was significantly lower than that in benign ovarian tumor tissues (40% P0.05) and normal ovarian tissues (60% P0.05). (2) the positive expression rate of Id1 in drug-resistant ovarian cancer group was 95% significantly higher than that in sensitive group (P 0.05). The positive expression rate of HtrA1 in drug-resistant ovarian cancer group was significantly lower than that in sensitive group (5% vs 40%, P0.05). (3) preoperative CA125 level, pathological grade and lymph node metastasis were closely related to the expression of Idl and HtrA1 (P0.05). (4) there was a negative correlation between the expression of Idl and HtrA1 (r = -0.186, P = 0.045). Conclusion (1) the positive expression rate of Id1 in normal and benign ovarian tumor tissues is lower than that in ovarian cancer tissue. However, the expression of HtrA1 decreased with the malignant change of tissue. (2) Drug resistance increased with the increase of Id1 expression and the decrease of HtrA1 expression in epithelial ovarian carcinoma. (3) the high expression of Id1 and the low expression of HtrA1 were closely related to the chemotherapeutic resistance and prognosis of ovarian epithelial carcinoma.
【学位授予单位】:青岛大学
【学位级别】:硕士
【学位授予年份】:2014
【分类号】:R737.31
本文编号:2379087
[Abstract]:Objective to investigate the expression of Id1 (inhibitor of differentiation or DNA bindingl) and HtrA1 (high temperature requirement factorl) in ovarian carcinoma, benign ovarian tumor and normal ovarian tissue and their relationship with clinicopathological parameters. Methods (1) 40 cases of ovarian epithelial carcinoma (chemosensitive group: 20 cases, drug-resistant group: 20 cases), 10 cases of benign ovarian tumor tissue and 10 cases of normal ovarian tissue were collected. (2) the expression of Id1 and HtrA1 in epithelial ovarian carcinoma, benign ovarian tumor and normal ovarian tissue were detected by immunohistochemical SP method. (3) the patient's age, tumor size, preoperative CA125 value, preoperative ascites volume, histological type of tumor, pathological grade, clinical stage and lymph node metastasis were analyzed. The relationship between the above clinicopathologic parameters and the expression of Idl and HtrA1 was observed. (4) to investigate the expression of Id1 and HtrA1 in epithelial ovarian carcinoma. Results (1) the positive rate of Id1 expression in ovarian cancer tissue was 77.5, which was significantly higher than that in benign ovarian tumor tissue (40 ovarian tumor tissues) and normal ovarian tissue (30jiao. 05). The positive rate of HtrA1 expression in ovarian cancer tissues was 22.5%, which was significantly lower than that in benign ovarian tumor tissues (40% P0.05) and normal ovarian tissues (60% P0.05). (2) the positive expression rate of Id1 in drug-resistant ovarian cancer group was 95% significantly higher than that in sensitive group (P 0.05). The positive expression rate of HtrA1 in drug-resistant ovarian cancer group was significantly lower than that in sensitive group (5% vs 40%, P0.05). (3) preoperative CA125 level, pathological grade and lymph node metastasis were closely related to the expression of Idl and HtrA1 (P0.05). (4) there was a negative correlation between the expression of Idl and HtrA1 (r = -0.186, P = 0.045). Conclusion (1) the positive expression rate of Id1 in normal and benign ovarian tumor tissues is lower than that in ovarian cancer tissue. However, the expression of HtrA1 decreased with the malignant change of tissue. (2) Drug resistance increased with the increase of Id1 expression and the decrease of HtrA1 expression in epithelial ovarian carcinoma. (3) the high expression of Id1 and the low expression of HtrA1 were closely related to the chemotherapeutic resistance and prognosis of ovarian epithelial carcinoma.
【学位授予单位】:青岛大学
【学位级别】:硕士
【学位授予年份】:2014
【分类号】:R737.31
【参考文献】
相关期刊论文 前1条
1 张涛;江普查;;分化抑制因子Id1与恶性肿瘤血管生成的研究进展[J];郧阳医学院学报;2009年01期
,本文编号:2379087
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